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RNA-sequencing analysis of glucose and acetate regulated transcripts in glioblastoma cells

ABSTRACT: Our studies indicate that glucose and acetate can regulate histone acetylation by altering the acetyl-CoA concentrations in the cell. The purpose of this study was to to determine whether specific gene sets correlated with acetyl-CoA availability. We conclude that 10% of glucose-regulated genes are acetyl-CoA regulated genes (genes suppressed or induced by low glucose and reversed by acetate). Acetate usually regulated gene expression in the same direction as glucose, suggesting that acetyl-CoA is a key mediator of glucose-dependent gene expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE57488 | GEO | 2014/08/05

SECONDARY ACCESSION(S): PRJNA246544

REPOSITORIES: GEO

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RNA-sequencing analysis of glucose and acetate regulated transcripts in glioblastoma cells

Project description:Our studies indicate that glucose and acetate can regulate histone acetylation by altering the acetyl-CoA concentrations in the cell. The purpose of this study was to to determine whether specific gene sets correlated with acetyl-CoA availability. We conclude that 10% of glucose-regulated genes are acetyl-CoA regulated genes (genes suppressed or induced by low glucose and reversed by acetate). Acetate usually regulated gene expression in the same direction as glucose, suggesting that acetyl-CoA is a key mediator of glucose-dependent gene expression. The experiments were performed in quadruplicates for each condition with a total of 12 samples

2014-08-05 | E-GEOD-57488 | biostudies-arrayexpress

Acetate promotes T cell effector function during glucose restriction [ATAC-seq]

Project description:Competition for nutrients like glucose can metabolically restrict T cells and contribute to their hyporesponsiveness during cancer. Metabolic adaptation to the surrounding microenvironment is therefore key for maintaining appropriate cell function. For instance, cancer cells use acetate as a substrate alternative to glucose to fuel metabolism and growth. Here we show that acetate rescued effector function in glucose-restricted CD8+ T cells. Mechanistically, acetate promoted histone acetylation and chromatin accessibility, and enhanced IFN-γ gene transcription and cytokine production in an acetyl-CoA synthetase (ACSS)-dependent manner. Ex vivo acetate treatment increased IFN-γ production by exhausted T cells, while reducing ACSS expression in T cells impaired IFN-γ production by tumor-infiltrating lymphocytes and tumor clearance. Thus, hyporesponsive T cells can be epigenetically remodeled and reactivated by acetate, suggesting that pathways regulating the use of substrates alternative to glucose could be therapeutically targeted to promote T cell function during cancer.

2019-05-14 | GSE128592 | GEO

Acetate promotes T cell effector function during glucose restriction [RNA-seq]

2019-05-14 | GSE128591 | GEO

Acetate promotes T cell effector function during glucose restriction [ChIP-seq]

2019-05-14 | GSE128593 | GEO

Generation of Escherichia coli Enhanced Acetate Utilization through Compensatory ATP Consumption via Adaptive Laboratory Evolution

Project description:We carried out adaptive laboratory evolution of an E. coli strain lacking four genes (adhE, pta, ldhA, frdA) involved in acetyl-CoA consumption, allowing the efficient utilization of acetate as its sole carbon and energy source. The transcriptomes according to the medium status (M9 aceate, M9 glucose) of the evolved strain (SBA01) and its parent strain (DSM01) were compared using RNA-seq.

2020-09-15 | GSE157942 | GEO

Enzymatic transfer of acetate on histones from lysine reservoir sites to lysine activating sites (ChIP-Seq)

Project description:Histone acetylation, a post-translational modification associated with transcriptional activation, is governed by nuclear acetyl-CoA pools that can vary depending on the metabolic state of the cell. The metabolic enzyme acetyl-CoA synthetase 2 (ACSS2) is proposed to regulate nuclear acetyl-CoA levels, using local acetate to produce acetyl-CoA that is utilized for histone acetylation. We hypothesize that during gene activation, a local transfer of intact acetate occurs between histones to upregulate transcription via sequential action of epigenetic and metabolic enzymes. Here we present converging lines of evidence in support of this acetate transfer to serve rapid gene induction. Using stable isotope labeling, we detect local transfer of intact acetate between histone acetylation sites both in vitro using purified mammalian enzymes and in vivo using quiescence exit in Saccharomyces cerevisiae as a change-of-state model. We delineate the enzymatic components required for this transfer mechanism, finding that ACSS2, histone deacetylase and histone acetyltransferase enzymes are necessary for efficient acetyl-group transfer in vitro. We show that Acs2, the yeast orthologue of ACSS2, is recruited to the genome during quiescence exit, and observe dynamic changes of histone acetylation in the vicinity of Acs2 peaks in vivo. Strikingly, we find that Acs2 is preferentially associated with the most upregulated growth genes, suggesting that acetyl-group transfer might play an important role in increased gene expression. Overall, our data reveal direct transfer of acetate between histone lysine residues to facilitate rapid transcriptional induction, an exchange that may be critical during metabolic alterations and changes in nutrient availability.

2022-01-21 | GSE189445 | GEO

Enzymatic transfer of acetate on histones from lysine reservoir sites to lysine activating sites (RNA-Seq)

2022-01-21 | GSE189444 | GEO

Gene expression profling of Mycobacterium tuberculosis H37Rv and H37RvΔdosSΔdosT in 0.2% glucose/acetate under aerobic/hypoxic conditions

Project description:The present study reports the gene expression data of Mycobacterium tuberculosis H37Rv and H37RvΔdosSΔdosT (DKO) grown on 0.2 % acetate/glucose under aerobic/hypoxic conditions. Acetate was reported to be present in granulomas of Mycobacterium tuberculosis infected guinea pigs which are also hypoxic. By exposing Mycobacterium tuberculosis H37Rv and H37RvΔdosSΔdosT to different combinations of granulomatous stresses (acetate/glucose and aerobic/hypoxic conditions) alongwith other experimental data, we were able to delineate a new signaling pathway that activates DevR (DosR) regulon through Acetyl phosphate. The presence of two pathways highlights the importance of targeting DevR and not DevS/DosT for intercepting DevRST signalling cascade.

2019-01-01 | GSE117428 | GEO

RNA-seq of Paracoccus denitrificans Pd1222 and a ramB deletion mutant during growth on succinate and acetate

Project description:The alphaproteobacterium Paracoccus denitrificans Pd1222 has two different, yet functionally redundant acetyl-CoA assimilation routes: the Ethylmalonyl-CoA pathway (EMCP) and the glyoxylate cycle (GC). The EMPC and the GC each tightly control the balance between catabolism and anabolism by shifting flux away from the oxidation of acetyl-CoA in the tricarboxylic acid (TCA) cycle towards biomass formation. RamB (encoded by Pden_1365), a member of the ScfR family, is a transcriptional regulator in P. denitrificans Pd1222 that controls expression of GC. To analyze the role of RamB in the coordinated regulation of metabolic plasticity, we analyzed the global transcriptome of P. denitrificans Pd1222, as well as the ramB-deletion strain during mid-exponential growth phase on defined minimal medium with acetate or succinate as carbon sources.

2023-06-06 | E-MTAB-12482 | biostudies-arrayexpress

RNA sequencing of E. coli NCM3722 over the course of glucose to acetate growth transition

Project description:To understand the gene response during the glucose to acetate diauxic transition, we grew E. coli in minimal media with acetate and a small amount of glucose. Cells were collected and RNA was purified at different time points during the growth transition, including pre-shift (growth on glucose), 5 minutes, 15 minutes, 60 minutes and 120 minutes after glucose run-out, and steady state growth on acetate (post-shift).

2021-10-09 | GSE185426 | GEO

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